GATA-4/5/6, a subfamily of three transcription factors transcribed in developing heart and gut.

Laverrière, A; MacNeill, Colin; Mueller, C.W.; Poelmann, Robert E.; Burch, John; Evans, Todd

doi:10.1016/s0021-9258(17)31636-8

Cited by 508 publications

(40 citation statements)

References 40 publications

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“…Many of them, such as Tbx2/3, SoxD1, FoxK2, Runt, Krüppel-like, and GATA factors, are activated during embryogenesis or regeneration in other animals. Furthermore, the genes involved in the specification of endoderm and the digestive system formation during the development of animals, such as, in particular, Sox9, SoxD1 [106,107], GATA4/5/6 [108], and a number of other ones, are expressed only in dividing individuals. The presence of a large number of transcripts of genes involved in the differentiation regulation and morphogenesis is the evidence that holothurian's tissues begin preparing for the subsequent regeneration during fission.…”

Section: Preparation For Whole Body Regenerationmentioning

confidence: 99%

Molecular Aspects of Regeneration Mechanisms in Holothurians

Dolmatov

2021

Genes

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Holothurians, or sea cucumbers, belong to the phylum Echinodermata. They show good regenerative abilities. The present review provides an analysis of available data on the molecular aspects of regeneration mechanisms in holothurians. The genes and signaling pathways activated during the asexual reproduction and the formation of the anterior and posterior parts of the body, as well as the molecular mechanisms that provide regeneration of the nervous and digestive systems, are considered here. Damage causes a strong stress response, the signs of which are recorded even at late regeneration stages. In holothurian tissues, the concentrations of reactive oxygen species and antioxidant enzymes increase. Furthermore, the cellular and humoral components of the immune system are activated. Extracellular matrix remodeling and Wnt signaling play a major role in the regeneration in holothurians. All available morphological and molecular data show that the dedifferentiation of specialized cells in the remnant of the organ and the epithelial morphogenesis constitute the basis of regeneration in holothurians. However, depending on the type of damage, the mechanisms of regeneration may differ significantly in the spatial organization of regeneration process, the involvement of different cell types, and the depth of reprogramming of their genome (dedifferentiation or transdifferentiation).

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Section: Preparation For Whole Body Regenerationmentioning

confidence: 99%

Molecular Aspects of Regeneration Mechanisms in Holothurians

Dolmatov

2021

Genes

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“…All of the genes were found to be hypermethylated in multiple tumor types, and hypermethylation of several of these genes (CDH1, CDKN2A, and RASSF1) has been observed in all of these tumor types. An immediate initial observation upon compilation of this list was the high frequency of targeting of genes involved in normal development, including genes such as p16 which can regulate stem cell number and cell cycle functions, 21 GATA transcription factors which regulate differentiation, 22 morphogenesis control genes such as CDH1, and anti-apoptotic genes such as DAP-kinase. 3 The nature of some of the genes raised for us the question of whether a stem or precursor cell origin for cancer, and specifically the underlying epigenetic controls responsible for controlling expression of these genes in normal stem and progenitor cells, provide an explanation for the targeting of at least some genes for DNA hypermethylation and gene silencing during tumor initiation and progression.…”

Section: Introductionmentioning

confidence: 99%

Stem Cell Chromatin Patterns: An Instructive Mechanism for DNA Hypermethylation?

Ohm¹,

Baylin²

2007

Cell Cycle

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Epigenetic gene silencing, and associated promoter CpG island DNA hypermethylation, is an alternative mechanism to mutations by which tumor suppressor genes may be inactivated within a cancer cell. These epigenetic changes are prevalent in all types of cancer, and their appearance may precede genetic changes in premalignant cells and foster the accumulation of additional genetic and epigenetic hits. These epigenetically modified genes constitute important categories of tumor suppressor genes including cell cycle regulators, pro-differentiation factors, and anti-apoptotic genes, and many of these genes are known to play a role in normal development. While the silencing of these genes may play an essential role in tumor initiation or progression, the mechanisms underlying the specific targeting of these genes for DNA hypermethylation remains to be determined. The large numbers of epigenetically silenced genes that may be present in any given tumor, and the clustering of silenced genes within single cell pathways, begs the question of whether gene silencing is a series of random events resulting in an enhanced survival of a premalignant clone, or whether silencing is the result of a directed, instructive program for silencing initiation reflective of the cells of origin for tumors. In this regard, the current review stresses the latter hypothesis and the important possibility that the program is linked, at least for silencing of some cancer genes, to the epigenetic control of stem/precursor cell gene expression patterns.

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“…The heart is formed from the anterior splanchnic mesoderm of the embryonic plate. During gastrulation, mesodermal cells arise from the primitive streak, and migrate cranially and laterally to the notochord to form the cardiogenic plates expressing Nkx2.5 [10] and GATA4 [11]. The first sign of cardiomyocyte differentiation is seen in this region at Hamburger and Hamilton (HH) stage 8-9 in chick and between embryonic day (E) 6.5-7.5 in mice, when cardiac troponin-I (cTnI) and sarcomeric myosin (MF20) are first detected.…”

Section: Basic Cardiac Development and Anatomy Of The Oftmentioning

confidence: 99%

The Role of Cell Tracing and Fate Mapping Experiments in Cardiac Outflow Tract Development, New Opportunities through Emerging Technologies

Peterson

Kelder

Goumans

et al. 2021

JCDD

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Whilst knowledge regarding the pathophysiology of congenital heart disease (CHDs) has advanced greatly in recent years, the underlying developmental processes affecting the cardiac outflow tract (OFT) such as bicuspid aortic valve, tetralogy of Fallot and transposition of the great arteries remain poorly understood. Common among CHDs affecting the OFT, is a large variation in disease phenotypes. Even though the different cell lineages contributing to OFT development have been studied for many decades, it remains challenging to relate cell lineage dynamics to the morphologic variation observed in OFT pathologies. We postulate that the variation observed in cellular contribution in these congenital heart diseases might be related to underlying cell lineage dynamics of which little is known. We believe this gap in knowledge is mainly the result of technical limitations in experimental methods used for cell lineage analysis. The aim of this review is to provide an overview of historical fate mapping and cell tracing techniques used to study OFT development and introduce emerging technologies which provide new opportunities that will aid our understanding of the cellular dynamics underlying OFT pathology.

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GATA-4/5/6, a subfamily of three transcription factors transcribed in developing heart and gut.

Cited by 508 publications

References 40 publications

Molecular Aspects of Regeneration Mechanisms in Holothurians

Molecular Aspects of Regeneration Mechanisms in Holothurians

Stem Cell Chromatin Patterns: An Instructive Mechanism for DNA Hypermethylation?

The Role of Cell Tracing and Fate Mapping Experiments in Cardiac Outflow Tract Development, New Opportunities through Emerging Technologies

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